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Biomedical subjects

V V Aristova

Publications and source records attributed to V V Aristova.

17 recordsLinked to original sources

HLDF-6 peptide relieves symptoms of abstinence syndrome during experimental opium abuse.

Experiments were performed on rats with opium abuse induced by chronic administration of morphine in increasing doses. We studied the effect of HLDF-6 peptide on symptoms of naloxone abstinence. Repeated administration of HLDF-6 peptide in a dose of 0.2 mg/kg 24 and 0.5 h before naloxone relieved the major symptoms of the abstinence syndrome. A possible neurochemical mechanism underlying the effect of HLDF-6 peptide is inhibition of enkephalinase A in structures of the endogenous antinociceptive system.

Animals↗

Use of HLDF-6 peptide for correction of disturbances in the endogenous opioid system in offspring of morphine-tolerant animals.

We studied the effect of bioactive peptide HLDF-6 on functional activity of the endogenous antinociceptive system in the offspring of morphine-tolerant animals. Disturbances in this system included changes in the thermonociceptive threshold and enkephalinase A activity in various brain structures. The peptide acted as a potent regulator of the homeostasis in systems responsible for the synthesis and catabolism of endogenous opioids. HLDF-6 effectively corrected disorders of the endogenous antinociceptive system.

Animals↗

Formation of morphine tolerance in offspring of morphine-tolerant animals: neurochemical and neuroimmune correlates.

We carried out a complex physiological, neurochemical, and neuroimmunologic study of the formation of tolerance to analgetic effect of morphine and analyzed enkephalinase A activity in different brain structures and serotonin antibodies in the serum. More early development of morphine tolerance and a sharp increase in serum antibody titer was found in the offspring of morphine-tolerant rats. This points to an imbalance in the neurotransmitter system and can serve as a diagnostic marker of endogenous opioid system pathology.

Analgesics, Opioid↗

Changes in thermonociceptive thresholds and the role of enkephalinase A in homeostasis in morphine-tolerant rat offspring.

The dynamics of thermonociceptive thresholds as a marker of the state of the endogenous opioid system was studied in the offspring of morphine-tolerant rats. Significant, age-dependent increase in thermonociceptive thresholds and higher levels of enkephalinase A in structures of the endogenous antinociceptive system were observed in the offspring compared with the control. These findings attest to disturbances of the opioid system in the progeny of morphine-tolerant rats and confirm the key role of enkephalinase A in the maintenance of homeostasis disturbed by chronic prenatal morphine treatment.

Animals↗

Action of beta-endorphin antiserum of different antibody titres on thermal or tail-shock pain in rats.

Intravenous injection of beta-endorphin antiserum (AS) with antibody titres of 1:1,600, 1:3,200, 1:12,800, and 1:20,000 decreased the voltage threshold in the tail-shock test (electrocutaneous nociceptive stimulus) in rats for 2 days, after which time control levels were regained. In the case of AS of titres 1:12,800 and 1:20,000 this threshold then increased to above control levels for about 40 and 100 days, respectively. This effect was abolished by naloxone. In the same rats, an injection of AS of titre 1:1,600 did not alter the latency of the tail-flick test (thermal nociceptive stimulus) but AS of titres 1:3,200, 1:12,800, and 1:20,000 decreased it for 1-4 h, the actual length of time being titre-dependent. After control levels had been regained, there was no further change in latency in the tail-flick test in the subsequent 42 days. Injection with preimmune serum did not change either voltage threshold or latency in the two tail-stimulation tests in control rats. Thus the hyperalgesic short-term effect seen in response to treatment with beta-endorphin AS was more pronounced in response to an electrocutaneous stimulus than to a thermal one, and the long-term selective analgesic effect was present in response to rats given electrocutaneous stimulation but not to thermal stimulation. It is proposed that beta-endorphin AS has a two-stage selective effect: a reduction in beta-endorphin release followed by a 'rebound' increase.

Animals↗

[The biphasic selective effect of an antiserum to beta-endorphin on pain sensitivity in rats].

In rats beta-endorphin antiserum systemic injection decreased during 1-2 days the threshold of tail-shock and latency of tail-flick tests, and during subsequent 85 days increased the threshold of tail shock, but not changed the latency of tail-flick tests. Naloxone injection blocked the increasing of thresholds, but not changed the latency of tail tests. It is suggested that antiserum evokes the first inhibition and the second selective activation of endogenous antinociceptive opioid system with affinity to electric nociception.

Animals↗

[A comprehensive study of the neurochemical and immune mechanisms of morphine tolerance: the effects of naloxone].

To test the authors' hypothesis about the role of endopeptidase (enkephalinase A, in particular) in mechanisms of morphine tolerance and blocking action of small doses of naloxone, they studied nociception reactions, morphine antibodies titres and enkephalinase A activity after morphine, d-phenylalanine and naloxone injection in brain structures. It is shown that activity of enkephalinase A in structures of endogenous antinociceptive system increased simultaneously with morphine antibodies titres in tolerance condition. Injection of small dose naloxone inhibited enkephalinase activity in brain structures and decreased morphine antibodies titres to these in control morphine-sensitive rats and therefore suppressed morphine tolerance. Prolonged naloxone injection decreased morphine antibodies titres to the levels of intact animals and highly increased titers of antiidiotypic morphine antibodies. Thus, these results confirm the role of enkephalinase as a neuromodulator. A strong relationship exists between enkephalinase and immune mechanisms of development of morphine tolerance which can be blocked by small naloxone doses. It is concluded that naloxone in small doses can be used in patients to suppress morphine tolerance.

Analgesics, Opioid↗

[The antihyperalgesic and selective analgesic effects of neurotropin].

In experiments of albino rats neurotropin injection was shown to increase the latency of the tail-flick test in response to the nociceptive thermal stimulus and didn't change the threshold of the test in response to the nociceptive electroskin stimulus. The administration of the antiserum to beta-endorphin lowered the threshold and the latency of the tail-flick test in response to both stimuli. The preliminary administration of neurotropin reduced the hyperalgesic effect of the antiserum on both nociceptive stimuli.

Analgesics↗

[The prolonged analgesic effect of an antiserum to beta-endorphin in rats].

Intravenous injection of beta-endorphin antiserum lowered the threshold of the tail-shock reaction to nociceptive electrocutaneous stimulation in rats in the first 1-2 days and raised it in the following 2-3 months. Naloxone injection reversed the analgesic effect of antiserum to beta-endorphin. Administration of normal serum did not change the threshold of the nociceptive reaction and naloxone failed to alter its effect. It is suggested that the secondary protracted effect of antiserum to beta-endorphin is a result of activation of the endogenous opioid system as a rebound-effect to diminished liberation of beta-endorphin in the first phase of the action of its antiserum.

Analgesics↗

[The action of neurotropin on the processes of conditioned-reflex avoidance in rats].

Preliminary neurotropin administration improved subsequent conditioned avoidance learning of rats in a shuttle-box: increased the number of conditioned avoidance reactions and decreased their latency in comparison with the control but did not change the number of intertrial responses. "The demolition" (5 series of negative reinforcements applied despite of avoidance occurrence) caused behavioural stress reactions and inhibited the conditioned and unconditioned avoidance learned reactions. Neurotropin injection before the demolition abolished such disturbances, that having been done after the demolition restored conditioned avoidance. The positive effects of neurotropin were suggested to be due to its antistress property and ability to improve the formation of a result of an acceptor of action.

Acoustic Stimulation↗

[Opioid mechanisms of the analgesic action of cocaine].

Rat experiments revealed a dose-dependent and naloxone-dependent analgetic effect of cocaine (0.5-3.0 mg/kg), evaluated by the tail-flick test. The cocaine-sensitive animals were morphine-sensitive and the cocaine-insensitive ones were morphine-insensitive. In some cocaine-insensitive rats, the use of cocaine led to that the first phase characterized by the lack of changes in nociception was followed by a hyperalgesic phase. It is suggested that cocaine produces an analgetic effect mainly via the delta-opioid mechanism.

Analgesics, Opioid↗

[Morphine antibodies in the mechanisms of morphine resistance, morphine tolerance and of the action of an antagonist].

It was found that the absence of the analgesic effect of morphine, as determined by the tail-flick test, in morphine-resistant and morphine-tolerant rats, as well as in naloxane blockade of morphine analgesia in morphine-sensitive rats was attended with a four- to eight-fold increase in morphine antibodies in the plasma, as determined by the ELISA method. It is suggested that a pharmacokinetic factor mediated through immune reactions of morphine antibodies formation is one of the mechanisms of such conditions.

Aging↗